Does a run/walk strategy decrease cardiac stress during a marathon in non-elite runners?

Abstract

Although alternating run/walk-periods are often recommended to novice runners, it is unclear, if this particular pacing strategy reduces the cardiovascular stress during prolonged exercise. Therefore, the aim of the study was to compare the effects of two different running strategies on selected cardiac biomarkers as well as marathon performance.DesignRandomized experimental trial in a repeated measure design.Methods
Male (n = 22) and female subjects (n = 20) completed a marathon either with a run/walk strategy or running only. Immediately after crossing the finishing line cardiac biomarkers were assessed in blood taken from the cubital vein. Before (−7 days) and after the marathon (+4 days) subjects also completed an incremental treadmill test.ResultsDespite different pacing strategies, run/walk strategy and running only finished the marathon with similar times (04:14:25 ± 00:19:51 vs 04:07:40 ± 00:27:15 [hh:mm:ss]; p = 0.377). In both groups, prolonged exercise led to increased B-type natriuretic peptide, creatine kinase MB isoenzyme and myoglobin levels (p < 0.001), which returned to baseline 4 days after the marathon. Elevated cTnI concentrations were observable in only two subjects. B-type natriuretic peptide (r = −0.363; p = 0.041) and myoglobin levels (r = −0.456; p = 0.009) were inversely correlated with the velocity at the individual anaerobic threshold. Run/walk strategy compared to running only reported less muscle pain and fatigue (p = 0.006) after the running event.Conclusions
In conclusion, the increase in cardiac biomarkers is a reversible, physiological response to strenuous exercise, indicating temporary stress on the myocyte and skeletal muscle. Although a combined run/walk strategy does not reduce the load on the cardiovascular system, it allows non-elite runners to achieve similar finish times with less (muscle) discomfort.KeywordsMarathonRecreational runnersCardiac troponinBrain natriuretic peptidePacing strategy

Full text

Please
cite
this
article
in
press
as:
Hottenrott
K,
et
al.
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
J
Sci
Med
Sport
(2014),
http://dx.doi.org/10.1016/j.jsams.2014.11.010
ARTICLE IN PRESS
G Model
JSAMS-1113;
No.
of
Pages
5
Journal
of
Science
and
Medicine
in
Sport
xxx
(2014)
xxx–xxx
Contents
lists
available
at
ScienceDirect
Journal
of
Science
and
Medicine
in
Sport
journal
h
om
epage:
www.elsevier.com/locate/jsams
Original
research
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
Kuno
Hottenrotta,b,∗,
Sebastian
Ludygab,
Stephan
Schulzea,b,
Thomas
Gronwalda,b,
Frank-Stephan
Jägerc
aDepartment
Sport
Science,
Martin-Luther-Universität
Halle-Wittenberg,
Germany
bInstitute
of
Performance
Diagnostics
and
Health
Promotion,
Martin-Luther-Universität
Halle-Wittenberg,
Germany
cCardiological
Clinic
Kassel,
Germany
a
r
t
i
c
l
e
i
n
f
o
Article
history:
Received
2
September
2014
Received
in
revised
form
15
October
2014
Accepted
7
November
2014
Available
online
xxx
Keywords:
Marathon
Recreational
runners
Cardiac
troponin
Brain
natriuretic
peptide
Pacing
strategy
a
b
s
t
r
a
c
t
Objectives:
Although
alternating
run/walk-periods
are
often
recommended
to
novice
runners,
it
is
unclear,
if
this
particular
pacing
strategy
reduces
the
cardiovascular
stress
during
prolonged
exercise.
Therefore,
the
aim
of
the
study
was
to
compare
the
effects
of
two
different
running
strategies
on
selected
cardiac
biomarkers
as
well
as
marathon
performance.
Design:
Randomized
experimental
trial
in
a
repeated
measure
design.
Methods:
Male
(n
=
22)
and
female
subjects
(n
=
20)
completed
a
marathon
either
with
a
run/walk
strategy
or
running
only.
Immediately
after
crossing
the
finishing
line
cardiac
biomarkers
were
assessed
in
blood
taken
from
the
cubital
vein.
Before
(−7
days)
and
after
the
marathon
(+4
days)
subjects
also
completed
an
incremental
treadmill
test.
Results:
Despite
different
pacing
strategies,
run/walk
strategy
and
running
only
finished
the
marathon
with
similar
times
(04:14:25
±
00:19:51
vs
04:07:40
±
00:27:15
[hh:mm:ss];
p
=
0.377).
In
both
groups,
prolonged
exercise
led
to
increased
B-type
natriuretic
peptide,
creatine
kinase
MB
isoenzyme
and
myoglobin
levels
(p
<
0.001),
which
returned
to
baseline
4
days
after
the
marathon.
Elevated
cTnI
con-
centrations
were
observable
in
only
two
subjects.
B-type
natriuretic
peptide
(r
=
−0.363;
p
=
0.041)
and
myoglobin
levels
(r
=
−0.456;
p
=
0.009)
were
inversely
correlated
with
the
velocity
at
the
individual
anaerobic
threshold.
Run/walk
strategy
compared
to
running
only
reported
less
muscle
pain
and
fatigue
(p
=
0.006)
after
the
running
event.
Conclusions:
In
conclusion,
the
increase
in
cardiac
biomarkers
is
a
reversible,
physiological
response
to
strenuous
exercise,
indicating
temporary
stress
on
the
myocyte
and
skeletal
muscle.
Although
a
combined
run/walk
strategy
does
not
reduce
the
load
on
the
cardiovascular
system,
it
allows
non-elite
runners
to
achieve
similar
finish
times
with
less
(muscle)
discomfort.
©
2014
Sports
Medicine
Australia.
Published
by
Elsevier
Ltd.
All
rights
reserved.
1.
Introduction
Benefits
of
regular
running
on
cardiorespiratory
fitness
are
known
to
reduce
all-cause
and
cardiovascular
mortality.1In
contrast,
sudden
death
in
marathon
runners
with
no
prior
doc-
umentation
of
heart
disease
shows
that
prolonged
endurance
exercise
can
have
the
opposite
effect
in
exceptional
cases.2
∗Corresponding
author.
E-mail
addresses:
kuno.hottenrott@sport.uni-halle.de
(K.
Hottenrott),
sebastian.ludyga@ilug.de
(S.
Ludyga),
stephan.schulze@sport.uni-halle.de
(S.
Schulze),
thomas.gronwald@sport.uni-halle.de
(T.
Gronwald),
info@kardio-praxis-ks.de
(F.-S.
Jäger).
Especially
in
recreational
endurance
runners
with
less
training
the
risk
for
cardiac
dysfunction
and
injury
is
increased
after
comple-
ting
a
marathon.3–5 In
this
respect,
the
steadily
growing
number
of
participants
in
running
events6emphasizes
the
need
to
assess
bio-
chemical
markers
that
allow
the
prediction
of
the
cardiovascular
risk
during
prolonged
exercise
at
submaximal
intensity.
Previous
studies
have
shown
that
prolonged
running
evokes
abnormal
elevations
in
creatine
kinase
MB
isoenzyme
(CK-MB),
cardiac
troponin
(cTnI),
and
B-type
natriuretic
peptide
(BNP).5In
clinical
settings,
increased
serum
levels
of
these
cardiac
mark-
ers
are
strong
prognostic
indicators
of
cardiac
events.3,7 However,
there
is
still
an
ongoing
debate
whether
elevations
in
CK-MB,
TNP
and
BNP
after
strenuous
exercise
reflect
irreversible
cardiac
damage
or
just
a
reversible
cardiac
fatigue.8–10 In
this
respect,
http://dx.doi.org/10.1016/j.jsams.2014.11.010
1440-2440/©
2014
Sports
Medicine
Australia.
Published
by
Elsevier
Ltd.
All
rights
reserved.

Please
cite
this
article
in
press
as:
Hottenrott
K,
et
al.
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
J
Sci
Med
Sport
(2014),
http://dx.doi.org/10.1016/j.jsams.2014.11.010
ARTICLE IN PRESS
G Model
JSAMS-1113;
No.
of
Pages
5
2
K.
Hottenrott
et
al.
/
Journal
of
Science
and
Medicine
in
Sport
xxx
(2014)
xxx–xxx
Fortescue
et
al.11 argue
that
high
BNP
and
TNP
concentrations
after
a
marathon,
particularly
in
non-elite
runners,
might
be
due
to
an
incomplete
myocardial
adaptation
to
training
in
which
vulnera-
ble
myocytes
are
selectively
eliminated.
Furthermore,
increases
in
cardiac
markers
correlate
with
post-race
diastolic
dysfunction,
increased
pulmonary
pressures
and
right
ventricular
dysfunction
after
2000
m
rowing.3
Compared
to
running,
walking
is
associated
with
lower
energy
expenditure
and
less
physiological
stress.12 Therefore,
fitness
experts
still
recommend
walking
breaks
to
make
novice
runners
complete
a
marathon
successfully
and
safely.13 Referring
to
the
stress
on
the
cardiovascular
system,
this
recommendation
is
hardly
based
on
evidence,
as
the
effect
of
intermittent
running
on
selected
cardiac
markers
has
not
been
investigated
yet.
However,
a
previous
study
has
shown
that
regular
walking
breaks
do
not
reduce
fatigue
and
muscular
stress
during
a
24
km
run,14 whereas
hormonal
(e.g.
testosterone
and
cortisol)
responses
seem
to
differ
from
contin-
uous
running.15 Furthermore,
a
high
variability
of
pacing
impairs
marathon
performance,16 possibly
due
to
a
higher
energy
demand,
which
is
associated
with
an
uneconomical
running
strategy.
The
aim
of
the
study
was
to
compare
the
effects
of
a
run/walk
strategy
(RWS)
vs
running
only
(RUN)
on
selected
markers
of
car-
diovascular
injury
and
stress
(CK-MB,
BNP,
cTnI
&
myoglobin)
as
well
as
marathon
performance.
Additionally,
it
was
examined
whether
or
not
the
pacing
strategy
during
a
marathon
influences
the
restoration
of
maximal
aerobic
performance.
Higher
serum
concentrations
of
CK-MB,
BNP
and
myoglobin,
which
are
associ-
ated
with
an
increased
cardiovascular
risk,
were
expected
after
the
run/walk
protocol
(RWS).
2.
Methods
In
response
to
a
newspaper
advertisement,
recreational
athletes
applied
for
the
study
by
submitting
personal
data
including
age,
weight,
profession
and
exercise
experience.
Only
runners
with
a
regular
training
volume
of
10–20
km/week,
who
did
not
participate
in
marathons
before,
were
included.
Exclusion
criteria
were
any
chronic
or
acute
cardiovascular,
neuronal
and
orthopedic
diseases
that
could
jeopardize
the
performance
and
safety
of
participants
during
the
marathon.
Prior
to
the
study
they
received
a
medical
check-up
including
a
detailed
personal
anamnesis,
ECG
at
rest
and
during
exercise,
echocardiography
as
well
as
measurement
of
blood
pressure.
At
baseline
cardiac
parameters
(BNP,
CK-MB,
cTnI
and
myoglobin)
were
assessed
in
a
venous
blood
sample.
Out
of
127
vol-
unteers,
48
male
and
female
recreational
runners
were
randomly
selected
to
participate
in
this
investigation.
The
anthropometric
data
of
the
study
participants,
who
completed
all
measurements,
are
shown
in
Table
1.
They
all
read
and
signed
an
informed-consent
approved
by
the
ethics
committee.
Prior
to
the
experimental
trial
participants
engaged
in
a
familiarization
period
including
three
months
of
aerobic
training
to
prepare
for
the
marathon
and
build
up
a
comparable
exercise
performance.
For
the
experimental
trial
recreational
athletes
were
randomly
assigned
to
two
groups
com-
pleting
a
marathon
either
by
running
only
(RUN;
n
=
21)
or
with
a
run/walk
strategy
(RWS;
n
=
21).
In
a
laboratory
setting,
participants
completed
exercise
testing
7
days
before
(baseline)
and
4
days
after
the
marathon.
At
rest,
a
blood
sample
was
taken
from
the
cubital
vein
to
assess
cTnI,
BNP,
CK-MB
and
myoglobin
levels.
The
blood
analysis
was
performed
with
MeterPro
(Alere
Triage,
Australia)
providing
high
sensitiv-
ity
by
using
a
99th
percentile
cTnI
with
a
cut
off
at
0.02
ng
ml−1.
Regarding
the
assessment
of
CK-MB,
myoglobin
and
BNP
the
applied
assay
uses
a
sensitivity
of
1.0
ng
ml−1,
5.0
ng
ml−1and
5
pg
ml−1,
respectively.
Following
the
assessment
of
body
composi-
tion
with
a
bioimpedance
device
(Data
Input,
BIA
2000s,
Germany),
participants’
aerobic
performance
was
measured
in
an
incremen-
tal
running
test
under
continuous
registration
of
the
heart
rate.
Therefore,
they
gradually
increased
speed
from
initial
7.0
km
h−1
by
1.5
km
h−1after
each
1200
m
until
exhaustion.
The
test
was
stopped
when
participants
were
unable
to
maintain
the
speed.
At
rest
and
after
each
increment,
lactate
and
glucose
concen-
tration
were
assessed
with
enzymatic-amperometic
method
(Dr.
Müller
Gerätebau,
SUPER
GL
Ambulance,
Germany)
in
10
␮l
blood
taken
from
an
earlobe.
Heart
rate,
lactate
and
glucose
concentra-
tion
were
processed
with
WinLactat
4.6
(Mesics
GmbH,
Germany)
to
derive
individual
target
zones
for
the
marathon.
Additionally,
the
Dickhuth17 model
was
applied
to
the
lactate-velocity
curve
to
determine
the
individual
aerobic
and
anaerobic
threshold.
Four
days
after
the
marathon
the
exercise
test
was
repeated
to
assess
whether
or
not
aerobic
performance
was
recovered
and
cardiac
markers
returned
to
baseline
levels.
All
recruited
recreational
runners
participated
in
the
EON
Mitte
Kassel
Marathon
(May
2013
in
Kassel,
Germany).
The
course
had
180.8
m
difference
in
altitude
including
a
maximal
incline
of
7%
over
a
distance
of
500
m
(starting
at
37
km).
Using
the
water
sta-
tions
as
reference,
the
RWS
switched
from
running
to
walking
every
2.5
km.
Each
walking
period
was
compromised
of
60
s
at
a
self-
chosen
velocity
in
which
participants
felt
comfortable.
In
contrast,
the
RUN
completed
the
marathon
by
running
only.
During
the
event
heart
rate
and
velocity
were
recorded
continuously
with
heart
rate
monitors
with
integrated
GPS
(RCX3
GPS,
Polar
Electro
GmbH,
Finland).
Immediately
after
crossing
the
finishing
line,
lactate
was
measured
in
10
␮l
blood
taken
from
an
earlobe
and
participants
were
asked
to
rate
muscle
pain
(5-point
scale:
0
=
none,
4
=
worst
pain)
and
exhaustion
(5-point
scale:
0
=
none,
4
=
extreme).
Addi-
tionally,
a
blood
sample
was
taken
from
the
cubital
vein
to
assess
cTnI,
BNP,
CK-MB
and
myoglobin.
The
statistical
analysis
was
performed
with
SPSS
Statistics
19.0.
In
advance,
the
Shapiro–Wilk
test
was
applied
to
check
whether
or
not
the
data
were
normally
distributed.
As
our
vari-
ables
followed
a
Gaussian
distribution,
analysis
of
variance
was
used
for
comparison
between
and
within
participants.
To
cal-
culate
possible
interaction
effects
between
groups
a
two-way
ANOVA
(factors:
group,
time)
with
repeated
measures
on
the
sec-
ond
factor
was
applied.
Cardiac
markers,
aerobic
performance,
heart
rate
and
blood
lactate
were
selected
as
dependent
vari-
ables.
By
using
Student’s
t
test
for
unpaired
samples
mean
and
maximal
heart
rates
during
marathon,
perceptual
measures
(self-
reported
muscle
pain
&
fatigue)
and
finish
times
were
compared
between
RWS
and
RUN.
Furthermore,
possible
relationships
between
cardiac
markers
(BNP
in
ng
l−1,
CK-MB
in
ng
ml−1&
myo-
globin
in
␮g
l−1)
and
performance
parameters
(maximal
velocity
in
km
h−1&
velocity
at
the
individual
anaerobic
threshold)
were
investigated
by
calculating
the
Pearson
correlation
coefficient.
The
level
of
significance
was
set
at
p
≤
0.05.
3.
Results
Due
to
cramps
two
participants
in
RUN
were
not
able
to
continue
running
and
cross
the
finishing
line.
The
RWS
and
RUN
completed
the
marathon
in
04:14:25
±
00:19:51
(hh:mm:ss)
and
04:07:40
±
00:27:15
(hh:mm:ss),
respectively.
The
difference
in
marathon
time
was
not
significant
between
the
groups
(F
=
0.80;
p
=
0.377).
Furthermore,
participants’
mean
(158
±
7
min−1vs
154
±
6
min−1;
F
=
2.22;
p
=
0.146)
and
maximal
heart
rate
(174
±
8
min−1vs
173
±
7
min−1;
F
=
2.22;
p
=
0.888)
did
not
differ
significantly
between
RWS
and
RUN.
The
average
marathon
speed
was
correlated
with
velocity
at
the
individual
aerobic
(r
=
0.653;
p
<
0.001)
and
anaerobic
threshold
(r
=
0.761;
p
<
0.001)
as
well
as
the
maximal
velocity
during
the
treadmill
test
(r
=
0.805;

Please
cite
this
article
in
press
as:
Hottenrott
K,
et
al.
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
J
Sci
Med
Sport
(2014),
http://dx.doi.org/10.1016/j.jsams.2014.11.010
ARTICLE IN PRESS
G Model
JSAMS-1113;
No.
of
Pages
5
K.
Hottenrott
et
al.
/
Journal
of
Science
and
Medicine
in
Sport
xxx
(2014)
xxx–xxx
3
Table
1
Subjects’
characteristics.
RUN
(n
=
10
male/9
female)
RWS
(n
=
11
male/10
female)
Group
Group
*
sex
F
p
F
p
Age
(years)
46
±
6
44
±
8
0.61
0.441
0.05
0.825
Height
(cm)
172.5
±
8.5
173.4
±
6.9
0.12
0.735
1.01
0.323
Weight
(kg)
69.1
±
15.1
67.8
±
11.3
0.08
0.775
0.86
0.360
HRMAX (min−1) 180
±
11 179
±
9 0.14
0.710
1.87
0.181
VIANS (km
h−1)
11.5
±
0.9
11.8
±
1.1
0.64
0.430
0.20
0.661
VMAX (km
h−1)
13.4
±
1.3
14.0
±
1.4
1.85
0.182
0.01
0.923
HRMAX =
maximal
heart
rate;
VIANS =
velocity
at
individual
anaerobic
threshold;
VMAX =
maximal
velocity.
p
<
0.023).
Immediately
after
the
running
event,
participants
in
the
RWS
reported
less
muscle
pain
(1.3
±
1.1
vs
2.3
±
1.1;
p
=
0.006)
and
fatigue
(1.6
±
0.6
vs
±
2.3
0.8;
p
=
0.006)
despite
similar
marathon
times.
In
detail,
more
than
40%
of
RUN
reported
strong
to
extreme
exhaustion
compared
to
less
than
5%
of
RWS.
The
results
displayed
in
Table
2
confirm
a
global
effect
of
time
on
biochemical
markers.
From
baseline
(7
days
before
the
marathon)
to
the
assessment
immediately
after
the
marathon
BNP
(RUN:
324.5%;
p
=
0.013;
RWS:
267.2%;
p
<
0.001),
CK-MB
(RUN:
538.9%;
p
<
0.001;
RWS:
423.8%;
p
<
0.001)
and
myoglobin
(RUN:
1008.4%;
p
<
0.001;
RWS:
870.6%;
p
<
0.001)
increased
significantly
within
groups.
After
4
days
plasma
concentration
of
CK-MB
(RWS,
RUN:
p
<
0.001)
and
myoglobin
(RWS,
RUN:
p
<
0.001)
dropped
to
a
level
that
was
not
significantly
different
from
baseline.
Whereas
BNP
levels
in
RUN
remained
elevated
in
comparison
to
7
days
before
the
marathon
(p
=
0.146),
plasma
concentration
of
BNP
in
RWS
also
lowered
to
baseline
values
4
days
after
the
running
event
(p
<
0.001).
Over
the
measurement
time
points
the
concentration
of
biochemical
markers
was
not
significantly
different
between
groups.
The
cTnI
levels
of
all
participants
remained
below
the
detection
limit
of
0.05
ng
ml−1at
baseline
and
4
days
after
the
marathon.
The
running
event
did
not
cause
any
changes
in
cardiac
troponins,
apart
from
two
exceptions:
in
each
group
there
was
one
case
with
increased
cTnI
levels
immediately
after
finishing
the
marathon
(RWS:
cTnI
=
0.28
ng
ml−1;
RUN:
cTnI
=
0.15
ng
ml−1).
BNP
levels
immediately
after
the
marathon
were
inversely
cor-
related
with
velocity
at
the
individual
aerobic
(r
=
−0.363;
p
=
0.041)
and
anaerobic
threshold
(r
=
−0.364;
p
=
0.040).
Additionally,
there
was
a
correlation
between
plasma
concentration
of
myoglobin
and
velocity
at
the
individual
aerobic
threshold
(r
=
−0.456;
p
=
0.009).
Among
the
assessed
biochemical
markers
a
direct
relation
of
CK-
MB
and
myoglobin
levels
was
confirmed
(r
=
0.609;
p
<
0.001).
With
regard
to
perceptual
measures,
rating
of
muscle
pain
was
corre-
lated
with
postmarathon
concentration
of
myoglobin
(r
=
0.314;
p
=
0.033).
Compared
to
baseline
participants’
maximal
velocity
and
heart
rate
during
the
treadmill
test
was
lower
in
both
RWS
and
RUN
4
days
after
the
marathon.
In
contrast,
velocity
at
the
individual
anaerobic
threshold
and
maximal
blood
lactate
concentration
did
not
differ
significantly
between
the
measurements.
Furthermore,
the
results
displayed
in
Table
3
show
that
there
were
no
differences
in
aerobic
performance
and
exhaustion
criteria
between
RWS
and
RUN
at
pre-
and
post-marathon
assessments.
4.
Discussion
Despite
different
pacing
strategies,
both
groups
completed
the
marathon
with
no
differences
in
mean
heart
rate
and
finishing
time.
Consequently,
the
RWS
must
have
compensated
the
lower
veloc-
ity
during
the
walking
periods
with
a
higher
velocity
than
RUN
during
the
running
phases.
Due
to
the
decrease
in
limb
mechan-
ical
advantage
and
increase
in
knee
extensor
impulse,
running
requires
higher
metabolic
cost
than
walking.18 However,
similar
mean
and
maximal
heart
rates
between
the
groups
suggest
that
the
strain
on
the
cardiovascular
system
in
RWS
and
RUN
did
not
differ.
This
notion
is
further
supported
by
the
lack
of
differences
in
BNP,
CK-MB
and
myoglobin
levels
between
groups
immediately
after
the
marathon.
Despite
the
objectively
measured
cardiovascu-
lar
stress
was
similar
in
RWS
and
RUN,
muscle
pain
and
fatigue
was
rated
lower
by
runners
completing
the
marathon
with
the
run/walk
strategy.
In
general,
the
variation
of
pace
during
a
marathon
is
seen
as
intentionally
chosen
strategy
designed
to
minimize
the
physiolog-
ical
strain
during
strenuous
exercise
and
to
prevent
a
premature
termination
of
effort.19 However,
an
analysis
by
Haney
and
Mercer16 showed
that
best
marathon
performance
is
achieved
by
low
variations
in
running
velocity,
provided
that
athletes
choose
a
sustainable
initial
speed.20 Elite
athletes
are
considered
to
main-
tain
an
economical/efficient
running
strategy
with
few
variations
in
pacing.
In
contrast,
a
low
variability
of
pacing
in
the
RUN
compared
to
a
run/walk
strategy
(RWS)
did
not
elicit
performance
benefits.
Furthermore,
the
different
pacing
strategies
did
not
affect
recovery
as
RUN
and
RWS
completed
pre-
and
post-marathon
performance
assessments
with
no
significant
differences
between
groups.
How-
ever,
the
decreased
maximal
velocity
and
velocity
at
the
individual
anaerobic
threshold
post-marathon
as
well
as
BNP
and
CK-MB
lev-
els
remaining
above
baseline
indicate
that
participants
of
both
groups
were
not
able
to
fully
recover
in
4
days.
In
previous
studies
the
normalization
of
cardiac
markers
has
been
reported
one
to
two
weeks
following
a
marathon.4
Running
competitions
have
been
reported
to
elicit
temporal
abnormalities
in
cardiac
function.21 Similarly,
this
study
showed
a
transient
but
reversible
increase
in
cardiac
biomarkers
in
both
RWS
and
RUN
immediately
after
the
marathon.
As
elevations
in
BNP,
CK-
MB
and
myoglobin
were
inversely
correlated
with
velocity
at
the
individual
anaerobic
threshold,
the
increase
in
these
cardiac
mark-
ers
was
more
pronounced
in
runners
of
a
lower
training
status.
In
this
respect,
previous
studies
also
found
more
biochemical
and
echocardiographic
evidence
of
cardiac
injury
and
dysfunction
after
a
marathon
in
runners
of
low
fitness
levels.3,4,22,23 Siegel
et
al.23
even
consider
running
competitions
a
serious
risk
for
myocardial
infarction
and
cardiac
death,
particularly
in
the
elderly.
In
contrast,
Lucia
et
al.5found
no
evidence
of
cardiac
injury
despite
elevations
of
CK,
CK-MB
and
troponin-I.
In
the
present
study
the
observed
elevations
of
CK-MB
and
myo-
globin
levels
beyond
the
normal
range
are
consistent
with
the
results
of
previous
investigations.8,22 According
to
Saenz
et
al.24,
an
increased
concentration
of
CK-MB
and
myoglobin
reflect
acute
muscle
injury,
which
is
expected
from
prolonged
running,
due
to
exertional
rhabdomyolysis.
With
regard
to
myoglobin,
this
assumption
is
further
supported
by
the
present
study
results
as
a
correlation
between
postmarathon
myoglobin
concentration
and
self-reported
muscle
pain
has
been
confirmed.
Lippi
et
al.8also
attributed
rises
in
CK-MB
and
myoglobin
levels
to
reversible
mus-
cle
damage
rather
than
biochemical
signs
of
serious
myocardial

Please
cite
this
article
in
press
as:
Hottenrott
K,
et
al.
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
J
Sci
Med
Sport
(2014),
http://dx.doi.org/10.1016/j.jsams.2014.11.010
ARTICLE IN PRESS
G Model
JSAMS-1113;
No.
of
Pages
5
4
K.
Hottenrott
et
al.
/
Journal
of
Science
and
Medicine
in
Sport
xxx
(2014)
xxx–xxx
Table
2
Biochemical
markers
before
(pre),
immediately
after
the
marathon
and
4
days
after
the
marathon
(post)
in
the
RWS-
(n
=
21)
and
RUN-group
(n
=
19).
Group
Pre
(−7
days)
Marathon
Post
(+4
days)
Time
Time
*
group
p
p
BNP
(ng
l−1)RWS
11.6
±
8.3 31.0
±
25.3
17.8
±
16.6 <0.001
0.416
RUN
10.6
±
6.3
34.4
±
22.8
15.2
±
19.7
CK-MB
(ng
ml−1)RWS
2.1
±
1.7
8.9
±
6.4*2.4
±
2.5 <0.001
0.936
RUN
1.8
±
1.0
9.7
±
6.9*2.3
±
1.3
Myo-globin
(␮g
l−1)RWS
46.9
±
25.0
408.3
±
134.5*58.8
±
33.7 <0.001 0.626
RUN
41.7
±
19.9
420.5
±
145.8*54.7
±
17.5
*Concentrations
were
elevated
above
the
physiological
range
defined
by
the
applied
assay
(CK-MB
>
4.7
ng
ml−1;
Myoglobin
>
107
␮g
l−1;
BNP
>
100
ng
l−1).
damage,
although
its
magnitude
resembles
the
elevations
observ-
able
after
acute
myocardial
infarction.25
Compared
to
CK-MB
and
myoglobin,
the
exercise-related
release
of
BNP
was
lower
after
the
marathon.
The
results
of
a
previous
study
imply
that
the
magnitude
of
the
increase
in
BNP
levels
depends
on
duration
rather
than
intensity.26 As
there
were
no
differences
in
marathon
time
between
RUN
and
RWS,
this
might
account
for
similar
elevations
in
BNP.
In
clinical
settings,
BNP
is
seen
as
a
strong
prognostic
indicator
of
cardiac
events
and
death
for
asymptomatic
patients
and
patients
with
heart
failure.7
The
exercise-related
increase
in
BNP
reported
in
multiple
stud-
ies
seems
to
be
physiological
rather
than
pathological.9However,
Neilan
et
al.3have
reported
a
strong
association
between
elevated
BNP
levels
and
the
postrace
development
of
cardiac
abnormalities
shown
on
two-dimensional
echocardiography.
In
this
respect,
the
authors
attributed
elevations
in
cardiac
biomarkers
to
changes
in
diastolic
filling,
reflecting
subtle
degrees
of
left
ventricular
dysfunc-
tion.
Saenz
et
al.24 suggest
that
increased
BNP
levels
might
reflect
a
physiological
response
to
natriuresis.
However,
a
lack
of
change
in
serum
sodium
despite
high
BNP
levels
does
not
support
this
theory.3
The
response
of
cardiac
troponin
levels
to
prolonged
running
varies
among
studies.
A
recent
meta-analysis
by
Regwan
et
al.10
showed
an
incidence
of
post-marathon
cTnI
elevation
in
51%
of
all
runners.
In
contrast,
a
lack
of
change
in
cTnl
levels
after
a
marathon
has
been
reported
by
other
authors.21,22 In
the
present
study,
pro-
longed
running
caused
elevations
in
cTnI
above
the
AMI
cut-off
(0.05
ng
ml−1)
in
only
two
cases.
Conventional
knowledge
suggests
that
this
increase
reflects
acute
myocardial
injury
indicative
of
myocardial
stunning
or
minor
myocardial
damage.21 According
to
Koller27,
the
kinetics
of
cTnI
release
might
be
explained
by
a
transient
increase
in
membrane
permeability,
so
that
cytosolic
troponins
leak
into
the
circula-
tion.
The
transitory
reversible
shift
in
membrane
permeability
could
be
due
to
a
stress-induced
overload
of
free
radicals.27
Furthermore,
a
relationship
between
cTnI
elevations
and
func-
tional
decrements
of
the
heart,
such
as
left
ventricular
dysfunction,
was
not
observable
in
the
majority
of
previous
studies.28 This
indicates
that
the
exercise-related
increase
in
cardiac
troponins
might
be
due
to
the
cytosolic
release
of
the
biomarker
and
not
to
the
true
breakdown
of
the
myocyte.10 Therefore,
several
authors
suggest
that
a
clinical
significance
of
exercise-related
elevations
in
cTnI
seems
unlikely.3,21 In
contrast
to
coronary
patients,
car-
diac
biomarkers
of
healthy
athletes
remain
within
the
normal
limit
at
rest,
increase
during
exercise
and
return
to
baseline
post-
exercise.29
The
present
results
have
to
be
interpreted
with
caution
as
this
study
is
not
without
limitations.
The
plasma
levels
of
car-
diac
biomarkers
might
have
been
influenced
by
participants’
fluid
intake,
which
was
not
assessed
in
the
study.
Possibly,
the
RWS
consumed
more
fluid
as
they
had
better
conditions
for
the
fluid
intake
during
the
walking
periods.
Furthermore,
the
present
results
do
not
allow
identifying
the
cause
of
elevated
cardiac
biomark-
ers.
As
electrolytes
were
not
assessed,
it
was
unclear
whether
or
not
the
increase
in
BNP
levels
was
due
to
natriuresis.
It
also
remains
unclear,
how
elevated
cardiac
biomarkers
were
related
to
functional
properties
of
the
heart,
because
echocardiography
was
not
performed.
Another
methodological
concern
was
the
use
of
the
Alere
system.
Although
it
provides
a
quick
assess-
ment
of
cardiac
biomarkers
and
can
be
used
in
field
tests,
the
exercise-related
elevations
of
BNP
were
restricted
by
the
upper
detection
limit.
Therefore,
the
real
magnitude
of
changes
in
car-
diac
biomarkers
after
a
marathon
might
have
been
higher
than
those
measured
in
the
study.
Moreover,
the
present
study
design
does
not
provide
full
insight
into
the
time-course
of
regeneration
after
a
marathon
event,
as
the
levels
of
CK-MB,
myoglobin,
BNP
and
cTnI
returned
to
baseline
after
4
days.
An
additional
assess-
ment
after
2
days
might
have
been
necessary
to
quantify
the
time-course
of
changes
in
cardiac
biomarkers
following
a
running
event.
Table
3
Aerobic
performance,
maximal
heart
rate
and
blood
lactate
concentration
7
days
before
(pre)
and
4
days
after
completing
the
marathon
(post)
with
different
pacing
strategies.
RUN
(n
=
19)
RWS
(n
=
21)
Time
Time
*
group
p
p
VMAX (km
h−1)Pre
13.4
±
1.3
14.0
±
1.4 0.002
0.753
Post
12.9
±
1.3
13.7
±
1.3
VIAS (km
h−1)Pre
9.5
±
0.8
8.6
±
0.7 <0.001
0.819
Post
9.6
±
0.6
8.8
±
0.6
VIANS (km
h−1)Pre
11.5
±
0.9
11.8
±
1.1 0.084
0.723
Post
11.2
±
0.9
11.7
±
1.0
LaMAX (mmol
l−1)Pre
6.55
±
1.50
7.22
±
1.65 0.430
0.831
Post
6.14
±
1.63
6.81
±
2.20
HRMAX (min−1)Pre
180
±
11
179
±
90.049
0.703
Post
178
±
10
174
±
7
HRMAX =
maximal
heart
rate;
VIAS =
velocity
at
individual
aerobic
threshold;
VIANS =
velocity
at
individual
anaerobic
threshold;
VMAX =
maximal
velocity;
LaMAX =
maximal
blood
lactate
concentration.

Please
cite
this
article
in
press
as:
Hottenrott
K,
et
al.
Does
a
run/walk
strategy
decrease
cardiac
stress
during
a
marathon
in
non-elite
runners?
J
Sci
Med
Sport
(2014),
http://dx.doi.org/10.1016/j.jsams.2014.11.010
ARTICLE IN PRESS
G Model
JSAMS-1113;
No.
of
Pages
5
K.
Hottenrott
et
al.
/
Journal
of
Science
and
Medicine
in
Sport
xxx
(2014)
xxx–xxx
5
5.
Conclusions
Prolonged
running
elicits
elevations
in
CK-MB,
myoglobin
and
BNP,
which
are
similar
to
those
of
patients
with
acute
myocardial
infarction.
Body
of
evidence
suggests
that
this
increase
in
cardiac
biomarkers
is
a
reversible,
physiological
response
to
prolonged
exercise,
indicating
temporary
stress
on
the
myocyte
and
skele-
tal
muscle
rather
than
long-term
damage
to
the
heart.
A
combined
run
walk
strategy
does
not
decrease
the
magnitude
of
these
eleva-
tions.
However,
lower
ratings
of
exhaustion
and
muscle
pain
after
the
marathon
despite
similar
finish
times
suggest
that
the
run
walk
strategy
reduces
the
load
on
the
muscoskeletal
system.
Therefore,
this
pacing
strategy
can
highly
be
recommended
to
non-elite
run-
ners,
as
similar
finish
times
can
be
achieved
with
less
discomfort.
After
the
marathon,
4
days
of
rest
are
sufficient
to
return
elevated
CK-MB,
BNP,
myoglobin
and
cTnI
concentrations
to
baseline
level.
The
clinical
significance
of
increased
levels
of
cardiac
biomarkers
still
remains
unclear
and
requires
further
investigation.
However,
exercise
behavior
must
be
taken
into
consideration,
when
CK-MB,
myoglobin,
BNP
and
cTnI
are
assessed
for
clinical
examinations.
6.
Practical
implications
•Prolonged
running
increases
levels
of
cardiac
biomarkers,
such
as
CK-MB,
BNP
and
myoglobin.
•Increased
levels
of
cardiac
biomarkers
return
to
baseline
4
days
after
the
marathon.
•Elevations
in
cardiac
biomarkers
are
not
reduced
by
a
run/walk
strategy.
•A
run/walk
strategy
reduces
perceived
fatigue
and
muscle
pain
in
recreational
endurance
runners.
Conflict
of
interest
None.
Acknowledgement
There
has
been
no
external
funding
to
support
the
experimental
trial.
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